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Updated 10:00 AM February 2, 2009
 

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  Research
Common infection may spread with help of protein

U-M researchers have discovered that a common parasite infecting one-in-five Americans needs an escape hatch to go on its destructive mission that can damage the brain, eyes and other organs.

The protozoan parasite Toxoplasma gondii infects up to 23 percent of Americans. In some areas of the world, up to 95 percent of the population serves as host to this parasite, which causes toxoplasmosis, a serious infection that can lead to birth defects, eye disease and life-threatening encephalitis.

In the cover story of the Jan. 23 issue of Science, researchers report the protein called TgPLP1 is responsible for helping the parasite spread infection. This research breakthrough may one day aid in developing drugs or vaccines to treat or prevent toxoplasmosis or related diseases, including malaria.

"For some time we've been interested in how this parasite successfully enters cells," says Vern Carruthers, the study's senior author and associate professor in the Department of Microbiology and Immunology at the Medical School.

"A couple of years ago, we identified several new proteins secreted by the parasite. Among these was TgPLP1, which captured our interest because it is related to proteins of our own immune system responsible for warding off infection and cancer," Carruthers says.

After the initial period of infection, which may cause mild flu-like symptoms, Toxoplasma gondii goes on to lie dormant in a person's brain and central nervous system. But if a person's immune system becomes compromised, such as from human immunodeficiency virus (HIV) infection or organ transplant surgery, the Toxoplasma infection can reactivate.

In an immunocompromised person, Toxoplasma gondii amplifies the infection by invading a cell and undergoing several rounds of replication within that cell. "Then it has to escape from the cell in order to find and infect additional cells," Carruthers says.

TgPLP1 is a type of protein responsible for forming pores, or small openings, in the cell membrane to allow the parasite to escape and more rapidly cause disease throughout the host.

Now that researchers know the purpose and importance of this protein for the disease, they may find ways of interfering with its functions, such as finding a selective treatment that disables the parasite protein and therefore slows or stops Toxoplasma gondii's spread.

This research may also offer insights into how the parasite that causes malaria, which kills more than 1 million people each year, might spread and cause infection.

"Because the malaria parasite has proteins similar to the one in the study, it may also use a pore-forming protein to escape from infected red blood cells," Carruthers says. Better understanding these mechanisms may someday help researchers develop new strategies for controlling the spread of the disease.

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